Purulent pleurisy

Classification and etiology

Purulent pleurisy is rarely primary (mainly in penetrating wounds). Depending on the location of the pus, free (total, moderate, small) and encysted pleurisy are distinguished. Encysted forms can be multilocular or unilocular (apical, parietal, basal, paramediastinal, interlobar).

Depending on the nature of the exudate, purulent, putrid, and purulent-putrid pleurisy are distinguished, as well as conditions with admixtures of air (pyopneumothorax) or blood (hemopyothorax).

Main causes of development:

• Lung abscess — the most frequent cause. Rupture of the abscess or lymphogenous infection may occur.
• Pneumonia — parapneumonic (at the peak of the disease) and metapneumonic (following resolution of pneumonia, more common) pleurisy.
• Gangrene of the lung — leads to the development of putrid inflammation.
• Trauma — infection of a hemopneumothorax.
• Extrapulmonary foci — appendicitis, pancreatitis, sepsis (infection is spread via lymphogenous or hematogenous routes).

A disease caused by mixed flora (e.g., Staphylococcus and Pneumococcus) has a significantly more severe clinical course.

Pathogenesis and complications

Upon penetration of highly virulent flora into the pleural cavity, hyperemia, edema, and abundant exudation begin. The pleura becomes covered with a layer of fibrin and infiltrated with leukocytes. The death of leukocytes leads to the formation of pus.

The exudate in the cavity has a characteristic stratification: transparent fluid is located at the top, liquid pus in the middle layer, and thick pus with crumbly masses of fibrin and detritus at the bottom. Deposition of fibrin promotes the agglutination of the pleural leaves, which can lead to encystment of the process.

Fluid accumulation causes compression syndrome: the lung is compressed, and the mediastinum is shifted toward the healthy side, which impairs hemodynamics and respiration.

Possible complications:

• Empyema necessitatis — melting of the parietal pleura and breakthrough of pus into the subcutaneous tissue of the chest wall.
• Bronchopleural fistula — melting of the bronchial wall.
• Development of dense fibrous tissue (pleural peels) when treatment is initiated late, leading to chronicity of the process and persistence of a residual cavity.
• Pleural shock — occurs during a sudden rupture of a subpleural abscess.

Clinical presentation and diagnostics

Symptoms depend on the volume of exudate and consist of signs of the underlying disease, purulent intoxication, and compression of adjacent organs.

• Complaints: at the onset of the process, patients are troubled by pronounced stabbing pain in the side, which is replaced by a feeling of heaviness and fullness as fluid accumulates. A persistent, nagging cough is characteristic, worsening at night when lying on the affected side.
• Objectively: the patient assumes a forced position (semi-sitting); acrocyanosis, tachypnea (up to 30–40 respiratory movements per minute), and lagging of the affected half of the chest during breathing are observed.
• Physical examination: vocal fremitus is weakened. Dullness is determined by percussion (with the upper boundary along the oblique Ellis-Damoiseau line), and Garland's and Grocco-Rauchfuss triangles are revealed. Breath sounds over the exudate are sharply weakened or absent.

Complete blood count shows leukocytosis, a left shift, and an elevated ESR. On the radiograph, exudative pleurisy presents an oblique line of opacification, whereas in pyopneumothorax (pus + free air), a horizontal fluid level is determined.

Principles of treatment and pleural puncture

The main goal of therapy is the contact and fusion of the pleural leaves with complete obliteration of the purulent cavity. The time factor is critical: early removal of pus prevents irreversible fibrous changes in the collapsed lung.

Treatment begins with diagnostic and therapeutic pleural puncture:

1. Puncture site: typically the 8th or 9th intercostal space between the scapular (l. scapularis) and posterior axillary (l. axillaris posterior) lines. In encysted processes, the site is determined radiologically.
2. Technique: after local anesthesia with a 0.5% procaine solution, a thick needle (1–2 mm) is advanced strictly along the upper edge of the underlying rib (to avoid damaging the intercostal vessels). Puncture of the parietal pleura is felt as a 'give' or 'loss of resistance'.
3. Equipment: the use of a three-way stopcock or a tube with a clamp is mandatory. This prevents the aspiration of atmospheric air and the development of iatrogenic pyopneumothorax.
4. Evacuation rules: pus should be removed slowly until negative pressure appears in the syringe. Rapid emptying causes a sharp drop in intrapleural pressure (ex vacuo hyperemia), rapid mediastinal shift, and can provoke shock.

Class and exam questions

What else to study on this topic

• Encysted forms of pleurisy: basal, apical, paramediastinal
• Physical phenomena: Garland's and Grocco-Rauchfuss triangles
• Formation of a residual cavity and chronicity of purulent pleurisy
• Bacteriological examination of exudate and principles of antibacterial therapy
• Surgical drainage and sanitation of the pleural cavity

Other topics from the section "CHAPTER 11. SURGICAL INFECTION (PURULENT-INFLAMMATORY DISEASES)"

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